In This Issue
Cancer Discov November 1 2015 5 (11) 1111-1113; DOI:10.1158/2159-8290.CD-ITI5-11
Clinically observed in-frame tandem duplication of the EGFR kinase domain is a recurrent oncogenic driver alteration in NSCLC and confers sensitivity to EGFR inhibitors.
Sequencing of matched primary tumors and brain metastases reveals branched evolution and frequent oncogenic alterations in potentially targetable pathways.
Loss of NF2 promotes thyroid tumorigenesis by increasing expression of both wild-type and mutant RAS in a YAP-dependent manner, resulting in enhanced dependency on MAPK signaling.
Association of the SIN1 PH domain with the mTOR kinase domain suppresses mTORC2 kinase activity, which is relieved by PtdIns(3,4,5)P3 binding to SIN1 or by cancer patient–derived SIN1 PH domain mutations that prohibit mTOR binding.
Integration of small-molecule cancer cell line sensitivity profiles with known drug targets and genomic features reveals context-driven vulnerabilities and small-molecule mechanisms of action.